• Childhood Kidney Diseases
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• v.23 no.1
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• pp.48-52
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• 2019

The ketogenic diet (KD) has been used as an effective antiepileptic therapy for intractable childhood epilepsy. However, various adverse effects have been reported with use of the KD. We report a case of a child who developed acute tubular necrosis subsequent to therapy with KD. A 5-year-old girl had myoclonic epilepsy with developmental delay. She was under the treatment with antiepileptic drugs since the age of 3 months and on the KD during the past 18 months. Proteinuria persisted intermittently with the initiation of the KD and subsequently increased in the past 2 months. She was admitted with intermittent mild fever, vomiting, and lethargy for the past 3-4 weeks. At the time of admission, she presented with hypertriglyceridemia, heavy proteinuria, renal Fanconi syndrome, and acute kidney injury. Renal sonography showed a marked increase in the size and parenchymal echogenicity of both kidneys. A renal biopsy revealed acute tubular necrosis accompanied by early interstitial fibrosis. After the withdrawal of the KD and supportive therapy, without changing other anticonvulsants and their dosages, improvement of renal function was observed. Proteinuria had disappeared after 1 month and kidney size returned to normal after 8 months. It is hypothesized that the KD can induce and/or aggravate the renal tubulointerstitial injury in some patients who are under the treatment with anticonvulsants.

• Clinical and Experimental Pediatrics
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• v.59 no.3
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• pp.145-148
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• 2016

Drug rash with eosinophilia and systemic symptoms (DRESS) syndrome is a rare and potentially fatal condition characterized by skin rash, fever, eosinophilia, and multiorgan involvement. Various drugs may be associated with this syndrome including carbamazepine, allopurinol, and sulfasalazine. Renal involvement in DRESS syndrome most commonly presents as acute kidney injury due to interstitial nephritis. An 11-year-old boy was referred to the Children's Hospital of Pusan National University because of persistent fever, rash, abdominal distension, generalized edema, lymphadenopathy, and eosinophilia. He previously received vancomycin and ceftriaxone for 10 days at another hospital. He developed acute kidney injury with nephrotic range proteinuria and hypocomplementemia. A subsequent renal biopsy indicated the presence of acute tubular necrosis (ATN) and late exudative phase of postinfectious glomerulonephritis (PIGN). Systemic symptoms and renal function improved with corticosteroid therapy after the discontinuation of vancomycin. Here, we describe a biopsy-proven case of severe ATN that manifested as a part of vancomycin-induced DRESS syndrome with coincident PIGN. It is important for clinicians to be aware of this syndrome due to its severity and potentially fatal nature.

• Korean Journal of Veterinary Research
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• v.16 no.1
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• pp.97-103
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• 1976

In order to clarify the histopathological changes resulting from nitrate poisoning, rabbits were experimentally poisoned by the oral administration of $KNO_3$ or $NaNO_2$ and examined clinically and histopathologically. In addition, the quantitative changes of glycogen level in hepatic cells were histochemically observed. The results obtained were summarized as follows: 1. Clinical symptoms observed from the acute cases which died within 2 hours after the administration were severe cyanosis of visible mucosa, frequent urination, and dyspnea. However, in chronic cases administrated daily with $KNO_3$ for 43, 50 and 74 days respectively, no marked symptoms were observed. 2. Macroscopic changes observed in acute cases were severe methemoglobinemia, cloudy swelling of hepatic cells, hemorrhage and hyperemia of gastric mucosa, and hyperemia of other organs. In chronic cases there were marked hyperemia, dark-red coloring and increasing of consistency in liver and kidney, and swelling of spleen. 3. Microscopic changes observed in acute cases were hemorrhage and hyperemia of various organs, cloudy swelling and centrilobular necrosis of hepatic cells and necrosis of convoluted tubular epithelium in kidney. In chronic cases there were round cell infiltration of the interlobular connective tissue and epithelial proliferation of interlobular bile ducts in the liver, and necrosis of the convoluted tubular epithelium and proliferation of interstitial connective tissue in kidney, thickening of alveolar septa of lungs, activated hemopoiesis of bone marrow, and myeloid metaplasia of sqlenic pulp. 4. Glycogen storage in liver cells was decreased in acute cases, on the contrary, increased in chronic cases.

• Childhood Kidney Diseases
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• v.1 no.1
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• pp.79-81
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• 1997

Minimal change nephrotic syndrome is characterized by proteinuria, hypoproteinemia, edema, and hyperlipidemia. Children with onset of nephrotic syndrome between the age of 1 and 8 year are likely to have steroid response to minimal chage disease, but we experienced one case of minimal change disease which failed to respond to steroid therapy at beginning and subsequently developed acute renal failure. It was seen in a 5 year-old male child that presented with edema and gross hematuria. Peritoneal dialysis was performed for acute renal failure for 11 days. Patient was completely recorvered from acute renal failure and renal biopsy was done at 27th day after onset of disease which revealed typical picture of minimal change disease complicated by acute tubular necrosis. We beleive this case is very unusual and it may be the first case in the literature in terms of pediatric cases.

• Journal of Yeungnam Medical Science
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• v.29 no.2
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• pp.145-149
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• 2012

Systemic capillary leak syndrome (SCLS) is an unusual entity characterized by hypovolemic shock, hemoconcentration, and hypo-albuminemia associated with paraproteinemia as a result of marked capillary hyper-permeability. Complications of this syndrome can include compartment syndromes, pulmonary edema, thrombosis, and acute kidney injury. This paper reports a case of severe SCLS accompanied by acute tubular necrosis caused by hypoperfusion and myoglobinuria secondary to rhabdomyolysis, which resulted in chronic kidney disease that necessitated hemodialysis. However, there have been rare data of residual end-organ damage after acute attacks in Korea. Therefore, this paper reports a case of complicated SCLS enough to hemodialysis and that developed into chronic kidney disease.

• Journal of fish pathology
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• v.36 no.2
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• pp.415-422
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• 2023

In veterinary medicine for mammals, studies are being conducted to confirm the effects of antioxidants using pathological toxicity model studies, and are also used to confirm the effect of mitigating liver or kidney toxicity of specific substances. It was considered necessary to study such a toxicity model for domestic farmed fish, so thioacetamide (TAA), a toxic substance that causes tissue damage by mitochondrial dysfunction, was injected into rainbow trout (Oncorhynchus mykiss), a major farmed freshwater fish species in Korea. The experiment was conducted with 40 rainbow trout (Oncorhynchus mykiss) weighting 53 ± 0.6 g divided into two groups. Thioacetamide(TAA) 300mg/kg of body weight was intraperitoneally injected into rainbow trout and samples were taken 1, 3, 5, 7 days after peritoneal injection. As a result, in serum biochemical analysis, AST levels related to liver function decreased 3 and 5 days after intraperitoneal injection and increased after 7 days, and ALT levels also increased after 7 days. In addition, creatinine related to renal malfunction increased 3 and 5 days after TAA injection. In histopathological analysis, pericholangitis and local lymphocyte infiltration were observed in the liver from 1 day after intraperitoneal injection of TAA, and hepatic parenchymal cell necrosis was also observed from 3 days after intraperitoneal injection. Hyaline droplet in renal tubular epithelial cell was observed from 1 day after TAA injection, and acute tubular damage such as tubular epithelial cell necrosis appeared from 3 days after TAA injection. Accordingly, it is thought that it will be able to contribute to studies that require a toxicity model.

• Nuclear Medicine and Molecular Imaging
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• v.42 no.3
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• pp.249-252
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• 2008

• Journal of Veterinary Science
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• v.21 no.6
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• pp.81.1-81.10
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• 2020

Background: Although previous in vivo studies explored urinary microRNA (miRNA), there is no agreement on nephrotoxicity-specific miRNA biomarkers. Objectives: In this study, we assessed whether urinary miRNAs could be employed as biomarkers for nephrotoxicity. Methods: For this, literature-based candidate miRNAs were identified by reviewing the previous studies. Female Sprague-Dawley rats received subcutaneous injections of a single dose or repeated doses (3 consecutive days) of gentamicin (GEN; 137 or 412 mg/kg). The expression of miRNAs was analyzed by real-time reverse transcription-polymerase chain reaction in 16 h pooled urine from GEN-treated rats. Results: GEN-induced acute kidney injury was confirmed by the presence of tubular necrosis. We identified let-7g-5p, miR-21-3p, 26b-3p, 192-5p, and 378a-3p significantly upregulated in the urine of GEN-treated rats with the appearance of the necrosis in proximal tubules. Specifically, miR-26-3p, 192-5p, and 378a-3p with highly expressed levels in urine of rats with GEN-induced acute tubular injury were considered to have sensitivities comparable to clinical biomarkers, such as blood urea nitrogen, serum creatinine, and urinary kidney injury molecule protein. Conclusions: These results indicated the potential involvement of urinary miRNAs in chemical-induced nephrotoxicity, suggesting that certain miRNAs could serve as biomarkers for acute nephrotoxicity.

• Proceedings of the Korean Society of Veterinary Pathology Conference
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• 2002.11a
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• pp.141-141
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• 2002

A patient (Painter+Viszula mixed breed, 4 months old, male), with chief historic sign of acute vomiting, hemorrhagic diarrhea, anorexia and dyspnea during 4 days was admitted ta College of Veterinary Medicine, Kyungpook National University. Necropsy findings were revealed ulcer and hemorrhage contained hemorrhagic diarrhea in gastrointestinal tract, severe emphysema and hemorrhage in the lung and kidney and cardiac hypertropy. Histopathological changes showed emphysema, hyperemia and hemorrhage in the lung, severe hyperemia, hemorrhage, hepatic vacuolation and cellular necrosis in the liver, hyperemia, hemorrhage, necrosis of tubular epithelium in the kidney, hemorrhage in cardiac muscle and hyperemia, necrosis and sloughing of epithelium in the intestine. In this case, we diagnosed as a paraquat poisoning.

• Journal of Veterinary Clinics
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• v.19 no.3
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• pp.379-382
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• 2002

A patient (Pointer+Viszula mixed breed, 4 months old, male), with chief historic sign of acute vomiting, hemorrhagic diarrhea, anorexia and dyspnea during 4 days was admitted to College of Veterinary Medicine, Kyungpook National University. Necropsy findings were revealed ulcer and hemorrhage contained hemorrhagic diarrhea in gastrointestinal tract, severe emphysema and hemorrhage in the lung and kidney and cardiac hypertropy. Histopathological changes showed emphysema, hyperemia and hemorrhage in the lung, severe hyperemia, hemorrhage, hepatic vacuolation and cellular necrosis in the liver, hyperemia, hemorrhage, necrosis of tubular epithelium in the kidney, hemorrhage in cardiac muscle and hyperemia, necrosis and sloughing of epithelium in the intestine. Histopathological diagnosis was made as paraquat poisoning.